Assessment of healthy trapeziometacarpal cartilage properties using indentation testing and contrast-enhanced computed tomography

BackgroundThe trapeziometacarpal joint is a common site for osteoarthritis development in the hand. When osteoarthritis is present, it results in significant functional disabilities due to the broad range of activities performed by this joint. However, our understanding of osteoarthritis initiation and progression at this joint is limited because of the current lack of knowledge regarding the properties and structure of the corresponding cartilage layers. The objective of this study is to assess the morphological and mechanical properties of trapeziometacarpal cartilage via the combination of indentation testing and contrast-enhanced computed tomography. Such research may lead to the development of medical imaging-based approaches to measure cartilage properties in vivo.MethodsIntact first metacarpals and trapezia were extracted from 16 fresh-frozen human cadaver hands. For each specimen, load-displacement behavior was measured at 9 testing sites using a standardized indentation testing device to calculate the normal force and Young's modulus of the cartilage sub-regions. The specimens were then immersed in CA4+ contrast agent solution for 48 h and subsequently scanned with a resolution of 41 μm in a HR-pQCT scanner to measure cartilage thickness and attenuation. Finally, correlations between compressive Young's modulus and contrast-enhanced computed tomography attenuation of the cartilage were assessed.FindingsNo significant difference was found in cartilage thickness between the trapezium and first metacarpal, but the comparison between articular regions showed thinner cartilage around the volar aspect of both the first metacarpal and the trapezium. The first metacarpal cartilage was stiffer than the trapezial cartilage. A significant positive correlation was observed between Young's modulus and mean contrast-enhanced CT attenuations in superficial and full-depth cartilage in both the first metacarpal and the trapezium cartilage.InterpretationThe quantitative measurements of trapeziometacarpal thickness and stiffness as well as a correlation between Young's modulus and contrast-enhanced computed tomography attenuation provides a method for the non-destructive in vivo assessment of cartilage properties, a greater understanding of thumb cartilage behavior, and a dataset for the development of more accurate computer models.     

关节镜下可吸收软骨钉治疗膝关节骨软骨损伤

背景：关节软骨骨折的手术治疗是骨关节外科常见难题,骨软骨骨折块缺乏有效的固定物,各种治疗方法的疗效也缺乏长期临床观察。目的：探讨关节软骨损伤在关节镜下采用可吸收软骨钉固定治疗的临床疗效。方法：纳入19例膝关节骨软骨缺损患者,在关节镜下修整损伤区及骨软骨骨折块以自身增强聚丙烯可吸收软骨钉固定,内固定后24h拔出负压引流管,抗生素预防感染不超过48h,充分镇痛条件下持续被动活动关节,膝关节铰链支具固定6周后完全负重行走。结果与结论：19例患者均获得3个月-2年随访,平均13.2个月。修复后患者2周-3个月恢复社会活动。膝关节Lysholm评分为（83.25±5.63）分,tegner运动评级6.1±0.87,修复前后配对t检验,差异有显著性意义（P〈0.05）。说明膝关节骨软骨损伤采用可吸收软骨钉固定可有效固定脱落的骨软骨块,促进软骨修复,改善膝关节功能。     

超声评估膝关节软骨退行性变的应用价值

目的:采用高频超声探查拟行关节镜手术及关节置换术的膝关节,评估超声对软骨退行性变的诊断效能。方法:选择2004-02/08在中山大学第三附属医院行膝关节镜手术患者36例37个膝关节及关节置换术患者4例4个膝关节。男13例,女27例,年龄8～75岁,病程1个月～20年。分别对每个膝关节的5个关节面,共计205个关节面的软骨进行高频超声探查,并将超声表现与关节镜结果及手术切除标本对照。结果:40例41个膝关节,均进入结果分析。超声诊断膝关节软骨退行性变的敏感性、特异性、准确性分别为64.9%,92.0%,76.5%。膝关节软骨退行性变超声表现为软骨表面毛糙、变薄或消失、局部隆起,回声改变和软骨下骨质改变等征象。结论:超声评估膝关节软骨退行性变具有一定的敏感性和较高的特异性,可作为诊断膝关节软骨退行性变的重要筛查手段。     

T2^*mapping技术评估早期膝关节软骨退变

目的:探讨T2^*mapping技术诊断早期膝关节软骨退变的应用价值。方法:常规MR成像显示关节软骨正常而关节镜诊断软骨退变的65个膝关节,先记录常规MR成像显示关节软骨正常的具体关节面和数量,再记录T2^*mapping诊断为软骨退变的具体关节面和数量并与关节镜结果对照。测量软骨内退变区域T2^*值以及正常区域T2^*值,统计分析两者是否存在差异。结果:65个膝关节,关节镜诊断软骨退变113处,T2^*mapping诊断软骨退变72处,T2^*mapping诊断阳性率63.7%。软骨退变区域的T2^*均值为30±8.1ms,正常区域的T2^*均值为23±5.1ms,差异有统计学意义(t=5.585,P<0.05)。结论:T2^*mapping技术可明显提高MR术前诊断早期软骨退变的阳性率。     

3.0T MR T1及T2 mapping评价肩关节软骨退变

目的 观察3.0T MR T1及T2 mapping在肩关节软骨退变中的应用价值.方法 对30例肩关节疼痛患者(患者组,34肩)和30名正常人(正常组)采用3.0T MR仪行肩关节常规、T1及T2 mapping序列扫描,按国际软骨修复协会(ICRS)分级标准对肩关节软骨分级,分别测量其外、中、内带T1及T2 mapp...     

兔膝关节软骨缺损对关节退变的影响

目的:探讨软骨损伤与关节退变之间的关系,以及持续被动运动治疗在其中的作用.方法:新西兰大白兔15只共30个膝关节随机分为3组,采用在关节软骨上钻孔的方法建立软骨损伤模型,术后按照不同的处理分为假手术组、对照组和持续被动运动(CPM)组,各组采取相应的处理方法.术后12周处死实验兔并进行关节软骨大体评分、HE染色评分和MMP-3免疫组化染色.结果:A组软骨表现正常.B组软骨在肉眼观察、病理学表现和MMP-3阳性细胞分数改变上均显示有明显退变.C组的各项指标均与A组接近而与B组差异有显著性意义(P＜0.05).结论:人为造成兔膝关节软骨缺损,可以进展成为骨关节炎(OA).软骨缺损后早期给予CPM治疗8h/d,连续4周,在12周后可有效减缓OA的发生.     

膝关节镜下治疗青少年盘状半月板损伤14例

目的探讨关节镜下青少年膝关节盘状半月板损伤的治疗方法及疗效。方法2002年2月～2006年1月,14例青少年膝关节盘状半月板损伤行关节镜下成形术,均为外侧盘状半月板,左10例,右4例,完全型8例,不完全型6例。男9例,女5例。年龄最小9岁,最大21岁,平均年龄15.2岁。结果14例获随访,随访8～22个月（平均13.6个月）,根据Ikeuchi膝关节评分标准,疗效优12例,良1例,可1例,优良率92.8%。按Lysholm评分方法术前术后功能评定疗效差异有显著性（P〈0.01）。结论关节镜下盘状半月板成形术创伤小,术后恢复快,是治疗青少年膝关节盘状半月板损伤的理想方法,主张尽可能施行关节镜下成形术治疗盘状半月板以保留半月板的生理功能,恢复接近正常生物力学状态,防止晚期关节退变。     

膝关节软骨退变的MRI与病理对照研究

目的:通过不同MR序列对膝关节软骨病变的检出与病理进行对照比较,总结适于软骨退变的MR检查方法。材料与方法:选择尸体膝关节9只,采用7种不同的序列进行扫描,即:FS 3D FAST、FS 3D RF-spoiled FAST、3D FAST、3D RF-spoiled FAST、SE T1WI、SE T2WI、SE PDWI。将各序列发现的病变数目及分级与病理结果进行对照,所有结果采用SPSS软件包进行统计学处理。结果:FS 3D FAST及FS 3D RF-spoiled FAST发现病变的敏感度为92%和95%,均优于其它MR序列,统计学结果显示与其它各序列比较有统计学显著性差异(P<0.05),而这两个序列的扫描结果之间无统计学显著差异(P>0.05)。结论:FS 3D FAST及FS 3D RF-spoiled FAST序列是发现软骨病变的敏感序列。     

关节腔注射几丁糖对兔关节软骨退变的影响

目的观察关节腔注射几丁糖对兔关节软骨退变的影响。方法18只大白兔行右膝关节前交叉韧带切断术建立骨关节炎（OA）动物模型。术后将动物随机分为2组，每组9只，实验组行2％几丁糖0．3m1关节腔注射，每2周1次，对照组同一时间点给予生理盐水0．3m1关节腔注射。第8周处死动物，比较两组兔股骨髁关节软骨的大体改变，用生化方法测定软骨基质蛋白多糖的变化，并用免疫组化方法对比两组的基质金属蛋白酶-1（MMP-1）的表达情况。结果实验组动物软骨退变程度轻于对照组（P〈0．05），氨基葡聚糖总量明显高于对照组（P〈0．01），硫酸软骨素／硫酸角质素比值低于对照组（P〈0．05），MMP-1的表达亦明显低于对照组（P〈0．01）。结论几丁糖能预防0A软骨退变，具有软骨保护作用。     

骨关节炎:关节软骨退变的相关研究与进展

背景:骨关节炎关节软骨退变被认为是不可逆的病理改变,但其病因及发病机制不清.目的:总结并探讨骨关节炎的病因、发病机制及相关的生物标志物的最新基础研究进展.方法:由第一作者用计算机检索中国期刊全文数据库(CNKI:2000/2010)和Medline数据库(2000/2010),检索词分别为"骨关节炎,关节软骨,退行性变,基础研究,生物标志物"和"Osteoarthritis,Articular cartilage,degradation,basic research,Biological markers",语言分别设定为中文和英文.从引起骨关节炎发病的相关因素的作用及相关的生物标志物的变化2方面进行总结,对病理、生物化学和免疫等相关因素及生物标志物的研究现状进行介绍.结果与结论:共检索到60篇文章,按纳入和排除标准对文献进行筛选,共纳入20篇文章.结果发现,关节软骨退行性变过程中可出现Ⅱ型原胶原羧基端前肽及Ⅱ型胶原羧基端肽等细胞因子的升高,基质金属蛋白酶、生物自由基、一氧化氮及细胞和体液免疫等参与了骨关节炎退行性变的过程,但其具体发病机制目前仍不明确.     

软骨终板细胞生物学特性及体外退行性变的机制研究

目的:通过建立猪腰椎间盘软骨终板细胞的培养模型,观察其演变,探讨软骨终板细胞的生物学行为及其影响因素。方法:取长枫杂交猪腰椎间盘软骨终板细胞,于200mL/L胎牛血清的杜尔伯克改良基础培养基(Dulbecco'smodifiedEagle'smedium,DMEM)中培养,建立体外软骨终板细胞培养模型。以光镜及苏木精-伊红染色观察其生物学表现;以甲苯胺蓝、番红O、Ⅱ型胶原免疫细胞化学染色对软骨终板细胞进行鉴定;观察冻存后软骨终板细胞的生物学特性。结果:原代细胞生物学性状最接近体内细胞,多次传代后细胞呈现衰老现象。经染色证实此细胞具有Ⅱ型胶原及蛋白多糖的表达。冻存细胞复苏后,细胞形态及其分化、增殖能力与冻存前基本相同。结论:猪腰椎软骨终板细胞的体外培养模型的建立,可为体外研究软骨终板的退行性变机制提供实验基础。     

Novel mechano-acoustic technique and instrument for diagnosis of cartilage degeneration

Fibrillation of articular surface and depletion of proteoglycans are the structural changes related to early osteoarthrosis. These changes make cartilage softer and prone to further degeneration. The aim of the present study was to combine mechanical and acoustic measurements towards quantitative arthroscopic evaluation of cartilage quality. The performance of the novel ultrasound indentation instrument was tested with elastomers and bovine articular cartilage in vitro. The instrument was capable of measuring elastomer thickness (r = 1.000, p < 0.01, n = 8) and dynamic modulus (r = 0.994, p < 0.01, n = 13) reliably. Osteochondral plugs were tested before and after enzymatic degradation of cartilage proteoglycans by trypsin or chondroitinase ABC, and of cartilage collagens by collagenase. Trypsin and collagenase induced a mean decrease of -31.2 +/- 12.3% (+/- SD, p < 0.05) and -22.9 +/- 20.8% (p = 0.08) in dynamic modulus, respectively. Rate of cartilage deformation, i.e. creep rate, increased by +117.8 +/- 71.4% (p < 0.05) and +24.7 +/- 35.1% (p = 0.17) in trypsin and chondroitinase ABC treatments, respectively. Collagenase induced a greater decrease in the ultrasound reflection from the cartilage surface (-54.2 +/- 29.6%, p < 0.05) than trypsin (-17.1 +/- 13.5%, p = 0.08). In conclusion, combined quantitation of tissue modulus, viscoelasticity and ultrasound reflection from the cartilage surface provides a sensitive method to distinguish between normal and degenerated cartilage, and even to discern proteoglycan loss and collagen degradation from each other.     

软骨延迟增强磁共振成像诊断膝关节软骨早期退行性变

目的 探讨dGEMRIC用于诊断膝关节软骨早期退变的可行性和价值.方法 OA组30例退变膝关节患者经肘静脉注射马根维显后步行10 min使对比剂尽量弥散至关节软骨内,注射后2 h接受dGEMRIC扫描;对照组27个正常膝关节.于T1时间图中选取感兴趣区(ROI)测量T1值,对照组同时测量软骨浅深层的T1值.对照组与OA组、对照组浅层与深层的T1值行独立样本t检验.结果 OA组的T1值为(359.10±41.64)ms,对照组为(426.42±39.81)ms,差异有统计学意义 (t=-6.223, P<0.05);对照组髌骨软骨浅层T1值为(411.39±41.50)ms,深层为(468.40±45.05)ms,差异有统计学意义 (t=-4.838, P<0.05).另于OA组5例患者的软骨T1时间图中发现低信号区.结论 dGEMRIC通过定量分析关节软骨中GAG含量的变化来判断关节软骨是否有组织成分的丢失,是可用于诊断关节软骨早期退变的有潜力的方法 .     

关节软骨病理损害的早期评价方法:MRI和关节镜图像对照

目的:比较膝关节软骨病理损害MRI和关节镜的影像学表现,探讨关节软骨变性和损伤的有效评价方法。方法:选择2003-01/2004-06在南京医科大学附属第一医院骨关节中心临床拟诊膝关节骨性关节炎、类风湿关节炎及其他关节紊乱症的患者125例,共148个膝关节,均行关节镜检查及MRI检查,将膝关节分髌骨、股骨内髁、股骨外髁、胫骨4个关节面,MIR图像和关节镜图像逐一对照分析。①关节软骨退行性变损害MRI分级采用Recht标准:0级正常关节软骨,Ⅰ级软骨分层结构消失,软骨内出现局灶性低信号区,软骨表面光滑,Ⅱ级软骨表面轮廓轻至中度不规则,软骨缺损深度未及全层厚度的50%,Ⅲ级软骨表面轮廓中至重度不规则,软骨缺损深度深达全层厚度的50%以上,但未见完全脱落,Ⅳ级软骨全层缺损、剥脱,软骨下骨质暴露伴或不伴软骨下骨质信号改变。②关节软骨退行性变损害的关节镜分级采用Outerbridge标准:0级正常关节软骨,Ⅰ级软骨软化水肿或出现表面泡状结构,Ⅱ级软骨变薄出现轻中度纤维化,Ⅲ级软骨重度纤维化,呈现蟹肉样改变,Ⅳ级软骨退行性变深达骨皮质,全层软骨缺损、软骨下骨质裸露。③分别统计592个关节面在MRI和关节镜的分级情况,然后使用统计软件SPSS10.0分析两者的一致性。结果:125例患者的148个膝关节(592个关节面)的MRI和关节镜图像资料均纳入分析。①膝关节软骨退行性变损害的MRI分级结果:0级11,Ⅰ级97,Ⅱ级171,Ⅲ级204,Ⅳ级109。②膝关节软骨退行性变损害的关节镜检查分级结果:0级11,Ⅰ级95,Ⅱ级146,Ⅲ级247,Ⅳ级93。③软骨退变损伤的MRI与关节镜对照分析结果:经一致性检验,kappa值0.674,统计量χ2=32.157,两者具高度一致性(P=0.000)。结论:磁共振和关节镜检查关节软骨各有其优势。在早期,当软骨病变局限于软骨内而表面无改变时,关节镜检查往往为阴性,磁共振可反映出软骨结构的改变。在晚期出现了软骨的变薄、脱落和骨质外露,关节镜观察更直观,能对软骨损伤的大小范围作出准确的判断,同时进行治疗。对关节镜治疗后的随访,效果评定,磁共振又能提供客观依据。只有MRI和关节镜检查结果相结合分析,对于关节软骨损伤的分类、分期及损伤范围、程度的评价才能为临床干预提供更加可靠的影像学信息。     

关节软骨病理损害的早期评价方法：MRI和关节镜图像对照

目的：比较膝关节软骨病理损害MRI和关节镜的影像学表现，探讨关节软骨变性和损伤的有效评价方法。方法：选择2003-01／2004-06在南京医科大学附属第一医院骨关节中心临床拟诊膝关节骨性关节炎、类风湿关节炎及其他关节紊乱症的患者125例，共148个膝关节，均行关节镜检查及MRI检查，将膝关节分髌骨、股骨内髁、股骨外髁、胫骨4个关节面，MIR图像和关节镜图像逐一对照分析。①关节软骨退行性变损害MRl分级采用Recht标准：0级正常关节软骨，Ⅰ级软骨分层结构消失，软骨内出现局灶性低信号区，软骨表面光滑，Ⅱ级软骨表面轮廓轻至中度不规则，软骨缺损深度未及全层厚度的50％，Ⅲ级软骨表面轮廓中至重度不规则，软骨缺损深度深达全层厚度的50％以上，但未见完全脱落，Ⅳ级软骨全层缺损、剥脱，软骨下骨质暴露伴或不伴软骨下骨质信号改变。②关节软骨退行性变损害的关节镜分级采用Outerbridge标准：0级正常关节软骨，Ⅰ级软骨软化水肿或出现表面泡状结构，Ⅱ级软骨变薄出现轻中度纤维化，Ⅲ级软骨重度纤维化，呈现蟹肉样改变，Ⅳ级软骨退行性变深达骨皮质，全层软骨缺损、软骨下骨质裸露。③分别统计592个关节面在MRI和关节镜的分级情况，然后使用统计软件SPSS10．0分析两者的一致性。结果：125例患者的148个膝关节（592个关节面）的MRI和关节镜图像资料均纳入分析。①膝关节软骨退行性变损害的MRI分级结果：0级11，Ⅰ级97，Ⅱ级171，Ⅲ级204，Ⅳ级109。②膝关节软骨退行性变损害的关节镜检查分级结果：0级11，Ⅰ级95，Ⅱ级146，Ⅲ级247，Ⅳ级93。③软骨退变损伤的MRI与关节镜对照分析结果：经一致性检验，kappa值0．674，统计量x^2=32．157，两者具高度一致性（P=-0．000）。结论：磁共振和关节镜检查关节软骨各有其优势。在早期，当软骨病变局限于软骨内而表面无改变时，关节镜检查往往为阴性，磁共振可反映出软骨结构的改变。在晚期出现了软骨的变薄、脱落和骨质外露，关节镜观察更直观，能对软骨损伤的大小范围作出准确的判断，同时进行治疗。对关节镜治疗后的随访，效果评定，磁共振又能提供客观依据。只有MRI和关节镜检查结果相结合分析，对于关节软骨损伤的分类、分期及损伤范围、程度的评价才能为临床干预提供更加可靠的影像学信息。     

Mechanobiology in the development, maintenance, and degeneration of articular cartilage

During skeletal development, the establishment of a layer of cartilage at the ends of long bones is intimately linked to the process of endochondral ossification. Previous in vivo studies and computer models suggest that mechanobiological factors can play a key role in modulating cartilage growth and ossification. Specifically, intermittent hydrostatic pressure is thought to maintain cartilage, and shear stresses encourage cartilage destruction and ossification. In the present investigation we examined the combined effects of hydrostatic pressure and shear stress--in the form of an osteogenic index--on the development of a layer of articular cartilage, using an idealized finite element computer model. The results of our analyses provide further support for the view that mechanobiological factors play a key role in regulating the distribution of cartilage thickness and in maintaining a stable cartilage layer at maturity. The model predicts that joints that experience higher contact pressures will have thicker cartilage layers. These predictions are consistent with observations of cartilage thickness in both humans and animals. Variations in articular mechanical load are predicted to modulate cartilage thickness. These results are consistent with the view that the mechanobiological factors responsible for the development of diarthrodial joints eventually lead to cartilage degeneration and osteoarthritis (OA) with aging.     

Reversibility of immobilization-induced articular cartilage degeneration after remobilization in rat knee joints

Joint immobilization is commonly used for the treatment of joint injuries, but it causes articular cartilage degeneration. The purpose of this study was to clarify the reversibility of immobilization-induced articular cartilage degeneration using rat knee joints. Immobilization of rat knee joints induces atrophic changes in the non-contact area, loss of chondrocytes in the contact area, and hypertrophy of chondrocytes in the transitional area of the articular cartilage. The unilateral knee joints of adult male rats were rigidly immobilized at 150° of flexion with a plate and screws for 1, 2, and 4 weeks. After the experimental periods, the fixation devices were removed and the rats moved freely for 16 weeks. Sham-operated rats were used as a control. Sagittal sections at medial midcondylar regions of the knee were assessed with histological and histomorphometric methods. Mechanical properties were assessed by measuring the sound speed with scanning acoustic microscope. Reduction of cartilage proteoglycan in the non-contact area was almost reversible, but hypertrophy of chondrocytes in the transitional area and loss of chondrocytes in the contact area were irreversible even at 1-week immobilization-remobilization group. Sound speed of the articular cartilage in the contact area was not restored. These results indicate that atrophic changes through decreased mechanical stress in the non-contact area were reversible, but loss of chondrocytes and hypertrophy of chondrocytes in the contact and transitional areas through increased mechanical stress by rigid immobilization were irreversible after remobilization. Clinicians should be aware that even a short-term rigid immobilization could cause irreversible articular cartilage damage.     

电针抑制骨性关节炎的炎症反应及延缓关节软骨退变

背景:研究表明电针能有效缓解骨性关节炎的临床症状。目的:观察电针抑制骨性关节炎的炎症反应及保护关节软骨的作用机制。方法:采用木瓜蛋白酶双膝关节腔注射复制SD大鼠骨性关节炎模型,建模成功后分别电针内、外膝眼(EX-LE4,EX-LE5)治疗5,15,30min/d。结果与结论:与模型组比较,经电针15,30min/d治疗的骨性关节炎模型大鼠血液中P物质及关节液中白细胞介素1、白细胞介素6、肿瘤坏死因子α和基质金属蛋白酶3的质量浓度明显减少(P<0.05),血液中瘦素及关节液中基质金属蛋白酶抑制因子1的水平明显增加(P<0.05),同时软骨退变的程度明显减轻(P<0.05,P<0.01)。证实电针能有效减轻大鼠膝骨性关节炎的炎症反应,延缓关节软骨的退变。     

Age-related macular degeneration: evaluation and treatment

Any patient age 50 or older with distorted vision or vision loss may have age-related macular degeneration and should be immediately referred to an ophthalmologist. Early diagnosis and treatment are essential to preserve the current level of vision. We outline risk factors, clinical signs, what happens to the retina, and what treatments are currently available, as well as recommendations about vitamin and mineral supplementation.